In the past several years, the αv integrin subfamily has been repeatedly found to be involved in tumor progression and angiogenesis. The aim of this study was to investigate the expression of the integrin αv subfamily in laryngeal squamous cell carcinoma (LSCC), and to correlate the expression rate with tumor biological behavior and angiogenesis of the LSCC. The integrin αv subfamily, including αv, β1, β3, β5, β6 and β8 subunits, was immunohistochemically found to be expressed in 64 patients with LSCC, and we analyzed the relationship between the expression rate and the clinicopathological stage of this cancer. Immunohistochemical staining for CD105 was carried out in the same group of the patients. The intratumoral microvessel density (IMVD) of the LSCC was calculated by CD105 staining, and the correlation between the IMVD and αv subfamily expression was discussed. The results showed that all members of the integrin αv subfamily could be detected in the LSCC. The expression rate of integrin αv and β5 subunits in primary cancer was significantly higher than in normal tissue, and their expression rate in the group with lymphatic metastasis was significantly higher than in the group without metastasis. The IMVD of the group with positive expression of αv and β5 subunits was significantly higher than in the group with negative expression, but there were no significant effects on the β1, β3, β6 and β8 subunits in these biological processes. In conclusion, the expressions of integrin αv and β5 subunits were significantly associated with lymphatic metastasis and angiogenesis of the LSCC. Among the members of integrin αv subfamily, integrin αvβ5 might play an important role in invasion and metastases of the LSCC, and it may become a valuable marker for the evolution of the LSCC.
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http://dx.doi.org/10.1016/j.prp.2012.11.001 | DOI Listing |
Nat Commun
September 2024
Genethon, 1 bis rue de l'internationale, Evry, France.
Current adeno-associated virus (AAV) gene therapy using nature-derived AAVs is limited by non-optimal tissue targeting. In the treatment of muscular diseases (MD), high doses are often required but can lead to severe adverse effects. Here, we rationally design an AAV capsid that specifically targets skeletal muscle to lower treatment doses.
View Article and Find Full Text PDFJ Biol Chem
July 2024
Department of Biochemistry and Microbiology, Institute for Quantitative Biomedicine, Rutgers University, Piscataway, New Jersey, USA.
Polymerizing laminins are multi-domain basement membrane (BM) glycoproteins that self-assemble into cell-anchored planar lattices to establish the initial BM scaffold. Nidogens, collagen-IV and proteoglycans then bind to the scaffold at different domain loci to create a mature BM. The LN domains of adjacent laminins bind to each other to form a polymer node, while the LG domains attach to cytoskeletal-anchoring integrins and dystroglycan, as well as to sulfatides and heparan sulfates.
View Article and Find Full Text PDFJ Adv Res
May 2024
Beijing Institute of Hepatology, Beijing Youan Hospital, Beijing 100069, China; Department of Science and Technology, Beijing Youan Hospital, Beijing 100069, China. Electronic address:
Introduction: The N-terminal domain of angiopoietin-like protein 3 (ANGPTL3) inhibits lipoprotein lipase activity. Its C-terminal fibrinogen-like (FBN) domain is a ligand of macrophage integrin αvβ3.
Objectives: ANGPTL3 might home to plaque where it directly regulates macrophage function via integrin αvβ3 for atherosclerosis progression.
Acta Biochim Biophys Sin (Shanghai)
May 2024
School of Basic Medicine, Central South University, Changsha 410078, China.
Adhesion molecules play critical roles in maintaining the structural integrity of the airway epithelium in airways under stress. Previously, we reported that catenin alpha-like 1 (CTNNAL1) is downregulated in an asthma animal model and upregulated at the edge of human bronchial epithelial cells (HBECs) after ozone stress. In this work, we explore the potential role of CTNNAL1 in the structural adhesion of HBECs and its possible mechanism.
View Article and Find Full Text PDFNanoscale
March 2024
Cancer Phage Therapy Group, Department of Brain Sciences, Faculty of Medicine, Imperial College London, London, UK.
The TRAIL (Tumour Necrosis Factor-Related Apoptosis-Inducing Ligand) is a promising candidate for cancer treatment due to its unique ability to selectively induce programmed cell death, or apoptosis, in cancer cells while sparing healthy ones. This selectivity arises from the preferential binding of the TRAIL to death receptors on cancer cells, triggering a cascade of events that lead to their demise. However, significant limitations in using the TRAIL for cancer treatment are the administration of the TRAIL protein that can potentially lead to tissue toxicity (off-target) and the short half-life of the TRAIL in the body which may necessitate frequent and sustained administration; these can pose logistical challenges for long-term treatment regimens.
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